Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of cells that expand during cancer, inflammation, and infection, and have the ability to suppress T-cell responses. These cells are a unique component of the immune system that regulate immune responses in healthy individuals and in various diseases. This review discusses the origin, mechanisms of expansion, and suppressive functions of MDSCs, as well as their potential for therapeutic targeting. MDSCs are derived from myeloid progenitors and immature myeloid cells, and their expansion is associated with pathological conditions such as cancer, infection, and autoimmune diseases. In these conditions, MDSCs are activated and upregulate immune suppressive factors such as arginase and inducible nitric oxide synthase, leading to increased production of reactive oxygen species (ROS) and nitric oxide (NO). These factors contribute to the suppressive activity of MDSCs, which can inhibit T-cell function and promote immune suppression. MDSCs have been identified in various contexts, including cancer, bacterial and parasitic infections, acute and chronic inflammation, and autoimmune diseases. They can be divided into granulocytic and monocytic subsets, each with distinct functions and mechanisms of action. Granulocytic MDSCs express high levels of ROS and low levels of NO, while monocytic MDSCs express low levels of ROS and high levels of NO. Both subsets can suppress T-cell function, but through different mechanisms. MDSCs suppress T-cell function through various mechanisms, including the metabolism of L-arginine, the production of ROS and NO, and the induction of T regulatory cells. These mechanisms are regulated by signaling pathways such as STAT3, STAT1, and NF-κB. MDSCs can also contribute to the development of regulatory T cells and the suppression of immune responses in various pathological conditions. Therapeutic targeting of MDSCs is an area of active research, with strategies aimed at promoting their differentiation into mature myeloid cells, inhibiting their expansion, or blocking their function. These approaches include the use of vitamin A and its metabolites, inhibitors of COX2 and phosphodiesterase-5, and chemotherapeutic drugs such as gemcitabine. These strategies have shown promise in reducing MDSC numbers and improving immune responses in cancer patients. Overall, MDSCs play a critical role in immune regulation and are involved in various pathological conditions. Understanding their biology and mechanisms of action is essential for developing effective therapeutic strategies to target them in cancer and other diseases.Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of cells that expand during cancer, inflammation, and infection, and have the ability to suppress T-cell responses. These cells are a unique component of the immune system that regulate immune responses in healthy individuals and in various diseases. This review discusses the origin, mechanisms of expansion, and suppressive functions of MDSCs, as well as their potential for therapeutic targeting. MDSCs are derived from myeloid progenitors and immature myeloid cells, and their expansion is associated with pathological conditions such as cancer, infection, and autoimmune diseases. In these conditions, MDSCs are activated and upregulate immune suppressive factors such as arginase and inducible nitric oxide synthase, leading to increased production of reactive oxygen species (ROS) and nitric oxide (NO). These factors contribute to the suppressive activity of MDSCs, which can inhibit T-cell function and promote immune suppression. MDSCs have been identified in various contexts, including cancer, bacterial and parasitic infections, acute and chronic inflammation, and autoimmune diseases. They can be divided into granulocytic and monocytic subsets, each with distinct functions and mechanisms of action. Granulocytic MDSCs express high levels of ROS and low levels of NO, while monocytic MDSCs express low levels of ROS and high levels of NO. Both subsets can suppress T-cell function, but through different mechanisms. MDSCs suppress T-cell function through various mechanisms, including the metabolism of L-arginine, the production of ROS and NO, and the induction of T regulatory cells. These mechanisms are regulated by signaling pathways such as STAT3, STAT1, and NF-κB. MDSCs can also contribute to the development of regulatory T cells and the suppression of immune responses in various pathological conditions. Therapeutic targeting of MDSCs is an area of active research, with strategies aimed at promoting their differentiation into mature myeloid cells, inhibiting their expansion, or blocking their function. These approaches include the use of vitamin A and its metabolites, inhibitors of COX2 and phosphodiesterase-5, and chemotherapeutic drugs such as gemcitabine. These strategies have shown promise in reducing MDSC numbers and improving immune responses in cancer patients. Overall, MDSCs play a critical role in immune regulation and are involved in various pathological conditions. Understanding their biology and mechanisms of action is essential for developing effective therapeutic strategies to target them in cancer and other diseases.